Effects of itaconic acid on neuronal viability and brain mitochondrial functions

2021 ◽  
Author(s):  
Danielius Umbrasas ◽  
Paulius Čižas ◽  
Odeta Arandarčikaitė ◽  
Tadas Vanagas ◽  
Vilmantė Borutaitė
Keyword(s):  
Itaconic Acid ◽  
Neuronal Viability ◽  
Mitochondrial Functions

scholarly journals Anti-Apoptotic and Antioxidant Activities of the Mitochondrial Estrogen Receptor Beta in N2A Neuroblastoma Cells

2021 ◽  
Vol 22 (14) ◽  
pp. 7620
Author(s):  
Ioannis Tsialtas ◽  
Achilleas Georgantopoulos ◽  
Maria E. Karipidou ◽  
Foteini D. Kalousi ◽  
Aikaterini G. Karra ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptors ◽  
Antioxidant Activities ◽  
Estrogen Receptor Beta ◽  
Direct Involvement ◽  
Neuronal Viability ◽  
Atp Production ◽  
N2a Cells ◽  
Mitochondrial Functions ◽  
Receptor Beta

Estrogens are steroid hormones that play a crucial role in the regulation of the reproductive and non-reproductive system physiology. Among non-reproductive systems, the nervous system is mainly affected by estrogens due to their antioxidant, anti-apoptotic, and anti-inflammatory activities, which are mediated by membranous and nuclear estrogen receptors, and also by non-estrogen receptor-associated estrogen actions. Neuronal viability and functionality are also associated with the maintenance of mitochondrial functions. Recently, the localization of estrogen receptors, especially estrogen receptor beta, in the mitochondria of many types of neuronal cells is documented, indicating the direct involvement of the mitochondrial estrogen receptor beta (mtERβ) in the maintenance of neuronal physiology. In this study, cell lines of N2A cells stably overexpressing a mitochondrial-targeted estrogen receptor beta were generated and further analyzed to study the direct involvement of mtERβ in estrogen neuroprotective antioxidant and anti-apoptotic actions. Results from this study revealed that the presence of estrogen receptor beta in mitochondria render N2A cells more resistant to staurosporine- and H2O2-induced apoptotic stimuli, as indicated by the reduced activation of caspase-9 and -3, the increased cell viability, the increased ATP production, and the increased resistance to mitochondrial impairment in the presence or absence of 17-β estradiol (E2). Thus, the direct involvement of mtERβ in antioxidant and anti-apoptotic activities is documented, rendering mtERβ a promising therapeutic target for mitochondrial dysfunction-associated degenerative diseases.

Innovative Adhesive Systems for Dental Giomer Restorations

2018 ◽  
Vol 69 (10) ◽  
Author(s):  
Ioana Hodisan ◽  
Cristina Prejmerean ◽  
Tinca Buruiana ◽  
Doina Prodan ◽  
Loredana Colceriu ◽  
...  
Keyword(s):  
Acrylic Acid ◽  
Itaconic Acid ◽  
Adhesive System ◽  
Adhesive Systems ◽  
Substantial Agreement ◽  
Dye Penetration ◽  
Strong Adhesion ◽  
Innovative Materials ◽  
Dental Applications

The aim of this work was to reduce microleakage in giomer restorations by using innovative materials in both adhesive systems and light-cured dental giomer. Two adhesive systems with different primers were investigated. The innovative compounds in the primers were acrylic acid (AA)/itaconic acid (IA) copolymer modified with methacrylic groups and AA/IA/N-acryloyl-L-leucine copolymer grafted with methacrylic groups. In addition, the investigated new giomer G contains a pre-reacted glass based on the latter copolymer. The commercial Beautifil II giomer and the FL-Bond II adhesive system were used for comparison. Microleakage was evaluated by determining the scores and percentages of dye penetration lengths after thermocycling of a series of light-cured dental giomer restorations performed on 42 premolars extracted for orthodontic reasons. A lower microleakage value was recorded for the adhesive system containing the AA/IA/N-acryloyl-L-leucine copolymer grafted with methacrylic groups than for the commercial adhesive, which was in substantial agreement with SEM and AFM investigations. In this case, remarkable dentin sealing and a strong adhesion at the giomer restoration�tooth interface was observed, and the innovative adhesive was proven to be promising for dental applications.

Inhibition of Autophagy Potentiated Hippocampal Cell Death Induced by Endoplasmic Reticulum Stress and its Activation by Trehalose Failed to be Neuroprotective

2019 ◽  
Vol 16 (1) ◽  
pp. 3-11
Author(s):  
Luisa Halbe ◽  
Abdelhaq Rami
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Er Stress ◽  
Cell Damage ◽  
Protective Mechanism ◽  
Unfolded Proteins ◽  
Neuronal Viability ◽  
Hippocampal Cell ◽  
Trigger Cell Death ◽  
Autophagy Inhibition

Introduction: Endoplasmic reticulum (ER) stress induced the mobilization of two protein breakdown routes, the proteasomal- and autophagy-associated degradation. During ERassociated degradation, unfolded ER proteins are translocated to the cytosol where they are cleaved by the proteasome. When the accumulation of misfolded or unfolded proteins excels the ER capacity, autophagy can be activated in order to undertake the degradative machinery and to attenuate the ER stress. Autophagy is a mechanism by which macromolecules and defective organelles are included in autophagosomes and delivered to lysosomes for degradation and recycling of bioenergetics substrate. Materials and Methods: Autophagy upon ER stress serves initially as a protective mechanism, however when the stress is more pronounced the autophagic response will trigger cell death. Because autophagy could function as a double edged sword in cell viability, we examined the effects autophagy modulation on ER stress-induced cell death in HT22 murine hippocampal neuronal cells. We investigated the effects of both autophagy-inhibition by 3-methyladenine (3-MA) and autophagy-activation by trehalose on ER-stress induced damage in hippocampal HT22 neurons. We evaluated the expression of ER stress- and autophagy-sensors as well as the neuronal viability. Results and Conclusion: Based on our findings, we conclude that under ER-stress conditions, inhibition of autophagy exacerbates cell damage and induction of autophagy by trehalose failed to be neuroprotective.

Optimization Strategies for Microbial Itaconic Acid Biosynthesis

2017 ◽  
Vol 6 (3) ◽  
Author(s):  
Laura van der Straat ◽  
Leo H. de Graaff
Keyword(s):  
Itaconic Acid ◽  
Acid Biosynthesis

scholarly journals Tracking Hydroplasticization by DSC: Movement of Water Domains Bound to Poly(Meth)Acrylates during Latex Film Formation

Polymers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 2500
Author(s):  
Sebastian M. Dron ◽  
Maria Paulis
Keyword(s):  
Itaconic Acid ◽  
Water Resistance ◽  
Film Formation ◽  
Latex Film ◽  
Water Molecules ◽  
Acrylate Copolymer ◽  
Volatile Organic ◽  
Minimum Film Formation Temperature ◽  
Latex Film Formation ◽  
Formation Step

The film formation step of latexes constitutes one of the challenges of these environmentally friendly waterborne polymers, as the high glass transition (TG) polymers needed to produce hard films to be used as coatings will not produce coherent films at low temperature. This issue has been dealt by the use of temporary plasticizers added with the objective to reduce the TG of the polymers during film formation, while being released to the atmosphere afterwards. The main problem of these temporary plasticizers is their volatile organic nature, which is not recommended for the environment. Therefore, different strategies have been proposed to overcome their massive use. One of them is the use of hydroplasticization, as water, abundant in latexes, can effectively act as plasticizer for certain types of polymers. In this work, the effect of three different grafted hydroplasticizers has been checked in a (meth)acrylate copolymer, concluding that itaconic acid showed the best performance as seen by its low minimum film-formation temperature, just slightly modified water resistance and better mechanical properties of the films containing itaconic acid. Furthermore, film formation monitoring has been carried out by Differential Scanning Calorimety (DSC), showing that itaconic acid is able to retain more strongly the water molecules during the water losing process, improving its hydroplasticization capacity.

Schisandrin Restores the Amyloid β-Induced Impairments on Mitochondrial Function, Energy Metabolism, Biogenesis, and Dynamics in Rat Primary Hippocampal Neurons

Pharmacology ◽  
2021 ◽  
pp. 1-11
Author(s):  
Zhongyuan Piao ◽  
Lin Song ◽  
Lifen Yao ◽  
Limei Zhang ◽  
Yichan Lu
Keyword(s):  
Energy Metabolism ◽  
Cytochrome C ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Hippocampal Neurons ◽  
Citrate Synthase ◽  
Mitochondrial Permeability Transition ◽  
Amyloid Β ◽  
Mitochondrial Functions ◽  
Primary Hippocampal Neurons

Introduction: Schisandrin which is derived from Schisandra chinensis has shown multiple pharmacological effects on various diseases including Alzheimer’s disease (AD). It is demonstrated that mitochondrial dysfunction plays an essential role in the pathogenesis of neurodegenerative disorders. Objective: Our study aims to investigate the effects of schisandrin on mitochondrial functions and metabolisms in primary hippocampal neurons. Methods: In our study, rat primary hippocampal neurons were isolated and treated with indicated dose of amyloid β1–42 (Aβ1–42) oligomer to establish a cell model of AD in vitro. Schisandrin (2 μg/mL) was further subjected to test its effects on mitochondrial function, energy metabolism, mitochondrial biogenesis, and dynamics in the Aβ1–42 oligomer-treated neurons. Results and Conclusions: Our findings indicated that schisandrin significantly alleviated the Aβ1–42 oligomer-induced loss of mitochondrial membrane potential and impaired cytochrome c oxidase activity. Additionally, the opening of mitochondrial permeability transition pore and release of cytochrome c were highly restricted with schisandrin treatment. Alterations in cell viability, ATP production, citrate synthase activity, and the expressions of glycolysis-related enzymes demonstrated the relief of defective energy metabolism in Aβ-treated neurons after the treatment of schisandrin. For mitochondrial biogenesis, elevated expression of peroxisome proliferator-activated receptor γ coactivator along with promoted mitochondrial mass was found in schisandrin-treated cells. The imbalance in the cycle of fusion and fission was also remarkably restored by schisandrin. In summary, this study provides novel mechanisms for the protective effect of schisandrin on mitochondria-related functions.

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